Migraine, which is distinguished by moderate-to-severe headache attacks with autonomic symptoms of the nervous system, is a type of recurring, chronic, and disabling neurovascular disorder. Its prevalence is 12% in the general population and has the second rank of disabling neurological disorders [1], [2], [3], [4].

Migraine headaches can be triggered by the susceptibility of the brain to a possible genetic-based imbalance in external and internal homeostasis. As a result of the so-called trigger, trigeminovascular system activation leads to the secretion of neuropeptides and other molecules, which are responsible for local inflammation and strengthening of the neural system in the brainstem, trigeminal nucleus caudalis, thalamus, and cortex. This process results in sensitization to pain, worsening of symptoms, and disability of the central descending inhibitory system in activating itself or controlling the headache attacks [5], [6]. Another substantially discussed factor in the pathophysiology of migraine is cerebral and meningeal vasodilation, which can be affected by released mediators such as norepinephrine and calcitonin gene-related peptides. Furthermore, serotonin is of the mediators that are believed to play a key role in migraine pathophysiology with its possible low levels in-between the attacks and variable amount during attacks [4].

A various spectrum of medication is being utilized in the prophylaxis of migraine due to the fact that the current body of research lacks sufficient evidence over the underlying migraine headache mechanisms [5], [6]. Prophylactic treatment of migraine is predominantly aimed at reducing the frequency, duration, and severity of migraine attacks. Various considerations are taken into account over the selection of the medication, among which is the plausible side-effects of the prophylactic agent [5], [6], [7], [8]. Antidepressants are among the earliest types of medications with potential identified capabilities in preventing migraine attacks, particularly tricyclic antidepressants (TCAs) [9]. Amitriptyline (as a tricyclic antidepressant) is believed to have preventing mechanisms over the uptake levels of serotonin and norepinephrine. This characteristic simplifies the inhibitory effect in descending noxious such as endogenous pain control mechanisms that descend from the brainstem to the trigeminal nucleus caudalis. In addition, interacting with the endogenous adenosine system may inhibit the spreading of cortical depression [10]. Besides, due to the anticholinergic and antihistaminergic activities, it has the potential to justify its side effects. Sedation, weight gain, dry mouth, and constipation are among the most prevalent side effects of the so-called medications. Venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRIs), was found effective in a double-blind placebo-controlled trial [11] and a separate placebo-controlled trial [12]. 5-hydroxytryptamine, norepinephrine, and dopamine re-uptake is being inhibited by Venlafaxine. Even though it possesses a comparable mechanism of action to the TCA’s, it has the potential to further act expressly at the aforementioned receptors and does not bind the responsible receptors for the TCAs side effects [13], [14]. The current inquiry set out to put the prophylactic impacts and side effects of VLF and AMT into comparison in the individuals who suffer from migraine. The primary objective of the current trial was to evaluate AMT, as compared with VLF, for the prevention of headache frequency (attacks per month). The second objective was to gauge the effect of AMT, as compared with VLF, on attacks duration and intensity in migraineurs. The third objective was to compare the two study groups for any possible adverse drug reactions.

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